60 year old smoker patient came with epigastric pain and shortness of breath for 4 hours. The patient was tachypneic with SpO2 90%. Other vital signs were relatively stable. ECG was done, Troponin I was positive and CK-MB was 100 IU/l.
What is there in ECG above?
ST elevation and Q waves in lead II, III and avF with reciprocal ST depression in lead I, aVL, V5 and V6 which indicates Acute inferior wall STEMI.
Presence of elevated ST segments, tall T waves and absence of T wave inversion points towards the acuteness of ischemia.
There is an abnormal Q in II, III, aVF diagnostic and specific for an inferior infarct of indeterminate age. Although Q is not deep (>1/3rd of R wave), it is wide > 1 box, signifying a pathological Q. Had the wide Q been isolated in lead III, the Q wave wouldn’t be considered pathological.
Abnormal Q waves:
Q wider > 1 box (0.04 sec) and deeper > 1 box in 2 contiguous leads.
Q of any width before the precordial transition zone (i.e., V1-V3).
Q may have a QS shape, which is a very wide and deep Q wave usually indicative of MI, except in leads III or V1 +/-V2 where it may be represent a normal variant.
Wide +/- tall R in V1 or V2 indicates posterior MI.
What to look for in ECG?
Mnemonic for ST Elevation: ABCD ELEVATION
- Angina (prinzmental or vasospastic)
- Brugada syndrome (RBBB like pattern and ST elevation in right precordial leads – susceptible to VT and sudden cardiac death)
- Class Ic antiarrhythmics
- DC cardioversion
- Electrolytes (hyperkalemia)
- Left bundle branch block (LBBB)
- Early repolarization
- Ventricular aneurysm
- Acute pericarditis
- Takotsubo cardiomyopathy and Trauma (myocardial contusion)
- Infarction (AMI)
- Osborne “J” waves (hypothermia)
- Normal variant (male pattern – majority have concave ST elevation ≥1 mm in precordial leads; most marked in V2)
Causes of ST elevation and a way to differentiate between various causes has been discussed here: https://epomedicine.com/medical-students/ecg-changes-in-pericarditis/
Diagnosis of STEMI in ECG
Definition of STEMI:
- New ST elevation at the J point in two contiguous leads of >0.1 mV in all leads other than leads V2-V3
- For leads V2-V3 the following cut points apply: ≥0.2 mV in men ≥40 years, ≥0.25 mV in men <40 years, or ≥0.15 mV in women
Other conditions which are treated as a STEMI
- New or presumed new LBBB
- Isolated posterior MI
The presence of reciprocal ST depression helps confirm the diagnosis.
Evolution of ECG in Acute MI
- T wave is the first to change and last to normalize:
- 1st – “T” goes up (hyperacute tall T waves)
- then – “T” goes down (T wave inversion)
- lastly – “T” comes to place (T wave normalizes)
- ST elevation:
- Appears after T wave goes up
- Normalizes before T wave normalizes
- Q wave:
- Appears after ST elevation
- Never returns to normal (persists) – also seen in old MI
Localization of STEMI in ECG:
You really don’t need a mnemonic for this. Just remember that all the precordial leads are left-sided and hence, to detect the right sided infarction, we need to place the leads on right side of chest. As the precordial leads are placed sequentially to left, assign 2 precordial leads to each going from medial to lateral:
- V1 and V2: Septum
- V3 and V4: Anterior part of left ventricle
- V5 and V6: Lateral part of left ventricle
For limb leads: If you need a mnemonic for this, I have one –
- aVF (‘F‘ stands for floor i.e. inferior part of left ventricle)
- aVL (‘L‘ stands for lateral i.e. lateral part of left ventricle)
Do you remember this eithovein’s triangle?
The axis goes from negative to positive. Look how:
- Lead II and III shows inferior part
- Lead I shows anterior part
Reciprocal changes in STEMI: PAILS mnemonic
- Posterior ST Elevation – Anterior ST depression
- Anterior ST Elevation – Inferior ST depression
- Inferior ST Elevation – Lateral ST depression
- Lateral ST Elevation – Septal ST depression
- Septal ST Elevation – Posterior ST depression
In Right sided infarction, you see reciprocal changes in V1-V4.
Cardiac markers in Acute MI
- Troponin I (Gold standard)
- Fatty acid binding protein (FABP) is the earliest marker of AMI (earlier than myoglobin).
- Troponin-I and CK-MB rises about the same time (no benefit of one over another for earlier detection).
- CK has 2 letters – rises as early as 2 hours and persists to 2 days (useful to detect reinfarction)
- TPnI has 3 letters – rises as early as 3 hours
- Troponin-I has 9 letters – persists upto 9 days
Causes of False Positive Troponin: CPRS
- Cardiac – failure, injury, pericarditis, cardiomyopathy
- Pulmonary embolism
- Renal failure
Scoring of MI for mortality in first 14 days
Mnemonic: AMERICA (7 points)
- Age >65 years
- Markers – increased
- ECG – ST segment changes
- Risk factors – 3 or more (age, family history, diabetes, high cholesterol, hypertension, smoking, obesity, sedentary lifestyle, metabolic syndrome)
- Ischemia – 2 or more anginal events in last 24 hours
- CAD – prior 50% coronary stenosis
- Aspirin – use in last week
- 0-1: 4.7%
- 2: 8.3%
- 3: 13.2%
- 4: 19.9%
- 5: 26.2%
- 6-7: 40.9%
What you need to do at Emergency room?
Immediate Managemet of Acute MI: MONARCH
- Reperfusion (thrombolysis or PCI)
What you need to be aware of in ICU?
Life-threatening complications of Acute MI: FEAR A MI
- Failure (heart failure)
- Effusion and tamponade
- Arrhythmia (AV block, VT)
- Aneurysm (ventricular)
- MI (Re-infarction)
What you need to send patient home with?
Overall treatment in Post-MI patients: ABCDE
- Aspirin, ACE inhibitors, Antianginals and Aldosterone antagonists (as per need of patient)
- Beta-blocker and Blood pressure control
- Cholesterol lowering and Cigarette stopping
- Diet and Diabetes control
- Education and Exercise
Review the pathophysiology of Ischemic heart dieasese here: https://epomedicine.com/medical-students/ischemic-heart-disease/
is currently working as a medical officer at a Government Hospital in Nepal. He searches for and share simpler ways to make complicated medical topics simple. He also loves writing poetry, listening and playing music and travelling.